2010
BRIT1/MCPH1 Is Essential for Mitotic and Meiotic Recombination DNA Repair and Maintaining Genomic Stability in Mice
Liang Y, Gao H, Lin S, Peng G, Huang X, Zhang P, Goss J, Brunicardi F, Multani A, Chang S, Li K. BRIT1/MCPH1 Is Essential for Mitotic and Meiotic Recombination DNA Repair and Maintaining Genomic Stability in Mice. PLOS Genetics 2010, 6: e1000826. PMID: 20107607, PMCID: PMC2809772, DOI: 10.1371/journal.pgen.1000826.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsDNA double-strand breaksDNA repairGenomic stabilityDNA damage response pathwayBRIT1/MCPH1Meiotic homologous recombinationDNA damage signalingDamage response pathwayRecruitment of RAD51Localization of RAD51Novel key regulatorRAD51 foci formationDouble-strand breaksIrradiation-induced DNA damagePrimary microcephaly patientsBRCT domainMutant spermatocytesBRCA2 complexMCPH1 functionDamage signalingMeiotic chromosomesChromosomal synapsisProphase IResponse pathways
2009
Replicative Senescence as an Intrinsic Tumor-Suppressor Mechanism
Chang S. Replicative Senescence as an Intrinsic Tumor-Suppressor Mechanism. 2009, 201-217. DOI: 10.1007/978-1-4419-1075-2_8.Peer-Reviewed Original ResearchDysfunctional telomeresGenomic instabilityIntrinsic tumor suppressor mechanismsDNA damage response pathwayProtein-DNA complexesDamage response pathwayTumor suppressor mechanismEukaryotic chromosomal endsEnds of chromosomesP53-dependent senescenceAbsence of p53Complex cytogenetic profileTriggers senescenceDDR pathwaysResponse pathwaysChromosomal endsReplicative senescenceTelomere dysfunctionCellular senescenceOnset of cancerTelomeresSenescenceCancer progressionEpithelial tissuesHuman carcinomas